For the past year, part of my project has been focused on the studies of beta alleles of Ustilago maydis, which is a basidiomycete fungus that causes corn smut disease. The beta alleles are responsible for the maintenance of the filamentous form of the fungus, which can propagate as haploid form that is nonpathogenic. Or when the two haplod strains fuse, the dikaryon is pathogenic. However, the beta locus is multiallelic; 33 strains with different beta alleles have been isolated from nature. It's most interesting that all possible pairwise combinations of haploid strains that carry different beta alleles produce the filamentous dikaryon which is infectious. Filamentous growth and pathogenic development are not initiated, however, if cells carry identical beta alleles. Recently, it has been shown that each beta allele encodes two proteins: bE and bW, and only bE and bW from different alleles can form heterodimers. It is proposed that this heterodimer formation is the direct cause of self/nonself recognition demonstrated by the fungus. My project involves the structural determination of the bE and bW proteins from 2 different alleles and studies of the interaction of the two proteins, thus elucidating the molecular mechanism of the self/non-self recognition, which seems to be very general in a variety of fungi. I have used the Computer Graphics Laboratory facilities and software to view the homeo-domain homologs of the two proteins in order to understand the secondary structures and analyse the physical interactions through the studies of hydrophobic surfaces and possible contacts. These exercises have been and will be very helpful for my research.